Psoriasis, atopic dermatitis, and contact dermatitis are examples of diseases of the skin generally known as inflammatory dermatoses. These diseases are typically characterized by inflammation in the epidermis and/or dermis, and improvements in the treatment of such diseases are needed.
For example, psoriasis is a genetically-transmitted disease characterized by hyperproliferation of keratinocytes, resulting in thick, scaly plaques on the skin surface, usually in areas of pressure, elbows, knees, buttocks. Psoriasis is generally characterized by marked proliferation of keratinocytes and cutaneous inflammation, histologically and immunologically mediated by a T cell mechanism. T cells play a primary role in the pathogenesis of psoriasis, specifically characterized by a subset of activated Th1 cells which result in the release of tumor necrosis factor alpha and interferon gamma, causing the keratinocytes to produce cytokines, chemokines, and adhesion molecules. These pro-inflammatory molecules amplify and continue the inflammatory cascade. It should be noted that tumor necrosis factor alpha activates pro-inflammatory transcription factors NfkB and STAT1, precipitating the majority of cytokine production. Cytokines can be produced by immune cells, but also keratinocytes and fibroblasts within the skin.
Atopic dermatitis is characterized by a similar inflammatory cascade, with activation of transcription factors and cytokine production. It should also be noted that atopic dermatitis is sometimes characterized by and worsened by bacterial infections. Atopic dermatitis is a specific form of eczema that is typically clustered in families, and is characterized by dry, itchy skin, associated with a disruption of the barrier function of the skin. It is also seen with other atopic syndromes such as asthma, and allergic rhinitis. Clinically, it is often characterized by secondary infections, e.g., with Staphylococcus aureus. 
Contact dermatitis or contact eczema is an inflammatory skin reaction due to contact with irritants or allergens, resulting in a clinically visible eruption of the affected skin.
Sepsis is driven by widespread tissue injury mediated by alterations in the biosynthesis of the free radicals nitric oxide and superoxide anion. The imbalance of these two free radical species produces major changes in the distribution of extracellular water, disrupts epithelial and endothelial tight junctions, impairs endothelial function and vascular smooth muscle tone, impairs microcirculatory blood flow, triggers pulmonary arterial hypertension, and raises endothelial permeability. In some cases, sepsis may progress to a state of circulatory collapse, with widespread tissue dysfunction and multiple organ failure prior to death.
Although NO is produced during sepsis via the inducible NO synthase (iNOS) isoform, paradoxically NO is deficient within the microcirculation, resulting in ischemia of critical tissues. NO deficiency results both from its consumption by O2− and its diminished synthesis by the endothelial NO synthase (ecNOS) isoform. O2− is correspondingly elevated due to its excessive production by uncoupled mitochondria and the enzymes NADPH oxidase, xanthine oxidase, and uncoupled ecNOS. The imbalance of NO and O2− directly impairs the ability of the arteriolar microcirculation to dilate, producing a biological cascade of ischemia, tissue dysfunction, hemodynamic collapse, and multiple organ failure.
Nitric oxide has also been implicated in inflammatory diseases such as osteoarthritis (see, e.g., Abramson, Arthritis Research & Therapy 2008, 10(Suppl 2):S2).